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202. Data from Vemurafenib Cooperates with HPV to Promote Initiation of Cutaneous Tumors

203. Supplementary Table 1 from Vemurafenib Cooperates with HPV to Promote Initiation of Cutaneous Tumors

207. Supplementary Figure 2 from Basal Subtype and MAPK/ERK Kinase (MEK)-Phosphoinositide 3-Kinase Feedback Signaling Determine Susceptibility of Breast Cancer Cells to MEK Inhibition

209. Supplementary Tables 1-6 from Basal Subtype and MAPK/ERK Kinase (MEK)-Phosphoinositide 3-Kinase Feedback Signaling Determine Susceptibility of Breast Cancer Cells to MEK Inhibition

214. Supplementary Tables 1-5 from PIK3CA Cooperates with Other Phosphatidylinositol 3′-Kinase Pathway Mutations to Effect Oncogenic Transformation

215. Supplementary Figure Legends 1-2 from Basal Subtype and MAPK/ERK Kinase (MEK)-Phosphoinositide 3-Kinase Feedback Signaling Determine Susceptibility of Breast Cancer Cells to MEK Inhibition

216. Data from Basal Subtype and MAPK/ERK Kinase (MEK)-Phosphoinositide 3-Kinase Feedback Signaling Determine Susceptibility of Breast Cancer Cells to MEK Inhibition

222. Drug-tolerant persister cancer cells are vulnerable to GPX4 inhibition

223. A Call for Discovery and Therapeutic Development for Cutaneous Neurofibromas

227. Contributors

229. Destabilizing NF1 variants act in a dominant negative manner through neurofibromin dimerization

231. Ras-dependent RAF-MAPK hyperactivation by pathogenic RIT1 is a therapeutic target in Noonan syndrome-associated cardiac hypertrophy

232. DDDR-06. NEUROFIBROMATOSIS TUMOR SUPPRESSORS COOPERATIVELY DRIVE TUMOR DE-DIFFERENTIATION AND MEK INHIBITOR RESISTANCE IN PERIPHERAL NERVOUS SYSTEM TUMORS

245. Structure of the SHOC2–MRAS–PP1C complex provides insights into RAF activation and Noonan syndrome

246. Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

248. Functional interactions between neurofibromatosis tumor suppressors drive Schwann cell tumor de-differentiation and treatment resistance

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